NURSE-MIDWIFERY CARE TO VULNERABLE POPULATIONS Phase I: Demographic Characteristics of the National CNM Sample

The purpose of this article is to describe the extent to which certified nurse-midwives (CNMs) provide care to vulnerable populations in the United States and the source of reimbursement for this care. The data were obtained from the first phase of a national study to address the characteristics of women served and cost of care provided by CNMs. Results were analyzed nationally and by American College of Nurse-Midwives regions. Certified nurse-midwives in all types of practices are providing care to women from populations that are vulnerable to poorer than average outcomes of childbirth because of age, socioeconomic status, refugee status, and ethnicity. Ninety-nine percent of CNMs report serving at least one group of vulnerable women, and CNMs in the inner city and rural practices serve several groups. The vast majority of CNMs are salaried; only 11% receive their primary income from fee-for-service. Fifty percent of the payment for CNM services is from Medicaid and government-subsidized sources whereas less than 20% comes from private insurance. Source of income varies by type of setting in which the CNM attends births. The results suggest that CNMs, as a group, make a major contribution to the care of vulnerable populations.     

Atypical Varicella Exanthems Associated With Skin Injury

Abstract: varicella is a common childhood disease with a typical exanthem. We present four children with severe, localized disease, all associated with some form of trauma to the skin during the incubation period: a 3½-year-old boy sustained wasp stings on the hand, a 5-year-old boy received extensive sun exposure, a neonate had latrogenic trauma to her arm, and a 13-year-old boy underwent knee arthroscopy and was wearing a cast. It is postulated that such injuries to the skin either allowed more virus-infected cells to enter the skin at the sites, or that factors such as insect venom and ultraviolet light altered local immunity to varicella zoster virus.     

S-adenosylmethionine increases erythrocyte ATP in vitro by a route independent of adenosine kinase

The mechanism by which S-adenosylmethionine (SAM) and adenosine (Ado) increase ATP levels in intact human erythrocytes in vitro has been compared. The use of erythrocytes from healthy controls and from subjects totally deficient in adenine phosphoribosyltransferase (APRT), plus inhibitors of adenosine kinase (AK) and adenosine deaminase (ADA) separately and together, has enabled us to demonstrate that this increment in ATP levels occurred via totally different metabolic routes. The results show that: (i) whilst the Ado-induced increment in ATP was AK dependent, that produced by SAM was independent of AK; and (ii) the SAM-induced increment in ATP was totally dependent on APRT and that some of the increment produced by Ado might also be APRT dependent. The above data are consistent with the metabolism of SAM to ATP by a route recently identified by us whereby ATP is formed from deoxyadenosine: namely binding to the enzyme S-adenosylhomocysteine hydrolase with subsequent release of adenine and further conversion to ATP via APRT.     

Interleukin-1 and cancer progression: the emerging role of interleukin-1 receptor antagonist as a novel therapeutic agent in cancer treatment

The tumor microenvironment consists of tumor, immune, stromal, and inflammatory cells which produce cytokines, growth factors, and adhesion molecules that promote tumor progression and metastasis. Of particular interest in this setting is interleukin-1 (IL-1), a pleiotropic cytokine with numerous roles in both physiological and pathological states. It is known to be up regulated in many tumor types and has been implicated as a factor in tumor progression via the expression of metastatic and angiogenic genes and growth factors. A number of studies have reported that high IL-1 concentrations within the tumor microenvironment are associated with a more virulent tumor phenotype. Solid tumors in which IL-1 has been shown to be up regulated include breast, colon, lung, head and neck cancers, and melanomas, and patients with IL-1 producing tumors have generally bad prognoses. The exact mechanisms by which IL-1 promotes tumor growth remain unclear, though the protein is believed to act via induction of pro-metastatic genes such as matrix metalloproteinases and through the stimulation of adjacent cells to produce angiogenic proteins and growth factors such as VEGF, IL-8, IL-6, TNFα, and TGFβ. The IL-1 receptor antagonist (IL-1ra) is a naturally occurring inhibitor to IL-1 and acts by binding to the IL-1 receptor without activating it. The protein has been shown to decrease tumor growth, angiogenesis, and metastases in murine xenograft models. Our focus in this review is to summarize the known data on the role of IL-1 in tumor progression and metastasis and the use of IL-1 inhibition as a novel therapeutic approach in the treatment of solid organ malignancies.     

Novel mutations in the thymidine kinase and DNA polymerase genes of acyclovir and foscarnet resistant herpes simplex viruses infecting an immunocompromised patient.

BACKGROUND: Mutations in the thymidine kinase (TK) and DNA polymerase (pol) genes of herpes simplex virus (HSV) may confer resistance to antiviral drugs, particularly in the context of immunosuppression induced by infection with the human immunodeficiency virus (HIV). OBJECTIVES: To characterise the HSV type 2 (HSV-2) TK and DNA pol genes in an immunocompromised patient with clinical resistance to both acyclovir and foscarnet. STUDY DESIGN: The TK and DNA pol genes of isolates obtained over a 2-year period from an AIDS patient with severe genital herpes infection were characterised both phenotypically and genotypically. RESULTS: HSV strains that were acyclovir resistant/foscarnet sensitive, acyclovir sensitive/foscarnet sensitive and acyclovir resistant/foscarnet resistant were isolated during this time. The TK gene of all the acyclovir resistant isolates contained a large 969 bp deletion which extended into a downstream untranslated region. The foscarnet resistance was associated with an S725G mutation in a conserved region (region II) of the herpesvirus DNA pol gene. CONCLUSIONS: Clinical and virological suppression of the infection was not always associated with subsequent reactivation with wild-type virus. Mutations of the nature we describe have not previously been reported occurring simultaneously in HSV strains isolated from patients treated with acyclovir and foscarnet.